Physiological Role of Targeting of the Receptor for Advanced Glycation End Products and Its Involvement in Severe Acute Pancreatitis
DOI:
https://doi.org/10.48047/n8gvaa42Keywords:
Amylase, Chemokines, Inflammation, Leukocytes, and PancreasAbstract
Leukocyte infiltration and damage to pancreatic acinar cells serve as key indicators of severe
acute pancreatitis (AP) [1]. However, the signaling pathways involved in pancreatic
inflammation and tissue damage remain unclear. This study explores the impact of inhibiting
the receptor for advanced glycation end products (RAGE) signaling in AP. We examined the
role of RAGE signaling by administering a RAGE inhibitor (anti-RAGE) (500 µg/kg) to C57BL/6
mice prior to inducing pancreatitis with taurocholate injection into the pancreatic duct. AntiRAGE treatment led to a reduction in blood amylase levels, neutrophil infiltration in the
pancreas, hemorrhage, and edema caused by taurocholate-induced pancreatitis. Additionally,
anti-RAGE administration lowered MPO activity in both the pancreas and lungs.
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